Chemical leukoderma: Fact or fancy

Cummings, Martin M.

doi:10.1016/1046-199x(95)90112-4

Cited by 45 publications

(27 citation statements)

References 17 publications

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“…Unexpectedly, high serum selenium levels have been recorded in NSV patients (60,61). Occupational contact vitiligo because of phenolic derivatives has been studied as a model for NSV (62)(63)(64). Avian models (65) and selected human inherited diseases associated with vitiligo may substantiate this theory (3).…”

Section: Melanocyte Destructionmentioning

confidence: 75%

A Critical Appraisal of Vitiligo Etiologic Theories. Is Melanocyte Loss a Melanocytorrhagy?

Gauthier

andre

Taı̈eb

2003

Pigment Cell Research

264

211

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Common generalized vitiligo is an acquired depigmenting disorder characterized by a chronic and progressive loss of melanocytes from the epidermis and follicular reservoir. However, the mechanism of melanocyte disappearance has never been clearly understood, and the intervention of cellular and humoral autoimmune phenomena as primary events remains unproven. In this review, is discussed the data supporting the major theories of vitiligo, namely melanocyte destruction (autoimmune, neural and impaired redox status) and melanocyte inhibition or defective adhesion. Based on recent morphologic findings in vivo supporting a chronic detachment and transepidermal loss of melanocytes in common generalized vitiligo, a new theory is suggested proposing melanocytorrhagy as the primary defect underlying melanocyte loss, integrating most of the possible triggering/precipitating/ enhancing effects of other known factors.

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Section: Melanocyte Destructionmentioning

confidence: 75%

A Critical Appraisal of Vitiligo Etiologic Theories. Is Melanocyte Loss a Melanocytorrhagy?

Gauthier

andre

Taı̈eb

2003

Pigment Cell Research

264

211

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“…4 Genetic predetermination is evident by the higher than expected number of patients who have affected primary family members, 5 whereas anecdotal evidence demonstrates a correlation between environmental factors and onset. In contact/occupational vitiligo, the environmental trigger is exposure to specific chemotoxins, which include phenol and catechol derivatives 6,7,8 such as 4-tert-butylphenol (4-TBP). 9 A number of these chemicals induce cellular oxidative stress.…”

mentioning

confidence: 99%

A Role for Tyrosinase-Related Protein 1 in 4-tert-Butylphenol-Induced Toxicity in Melanocytes

Manga

Sheyn

Yang

et al. 2006

The American Journal of Pathology

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Vitiligo presents with depigmented cutaneous lesions following localized melanocyte death. Multiple factors contribute to cell death, including genetically determined susceptibility to trauma, and environmental factors, such as exposure to 4-tert-butylphenol (4-TBP). We demonstrate that 4-TBP induces oxidative stress that is more readily overcome by melanocytes from normally pigmented individuals than from two individuals with vitiligo. The antioxidant catalase selectively and significantly reduced death of melanocytes derived from two individuals with vitiligo, indicating a role for oxidative stress in vitiligo pathogenesis. In normal melanocytes, oxidative stress results in reduced expression of microphthalmia-associated transcription factor (MITF). Melanocyte-stimulating hormone-induced expression of MITF protein caused increased sensitivity to 4-TBP, whereas sensitivity of melanomas correlated with MITF expression. MITF stimulates melanin synthesis by up-regulating expression of melanogenic enzymes such as tyrosinase-related protein-1 (Tyrp1). Although melanin content per se did not affect sensitivity to 4-TBP, expression of Tyrp1 significantly increased sensitivity. Melanocytes and melanomas that express functional Tyrp1 were significantly more sensitive to 4-TBP than Tyrp1-null cells. Thus, normal melanocytes respond to 4-TBP by reducing expression of MITF and Tyrp1. We hypothesize that melanocytes in vitiligo demonstrate reduced ability to withstand oxidative stress due, partly, to a disruption in

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“…Einige substituierte Phenole wie Monobenzylether des Hydrochinon (MHQ) führen lokal zum Zelltod der Melanozyten, und, da gut resorbierbar, kann MHQ auch zu systemischen Reaktionen wie einer Vitiligo führen [43]. Das in der Dermatologie dagegen auch therapeutisch eingesetzte Hydrochinon als nicht substituiertes Phenol weist diese Eigenschaft nicht auf und führt auch lediglich zu lokalen, nicht aber zu systemischen Verän-derungen [13,34]. Einige der depigmentierenden Substanzen sind gleichzeitig stark irritierend, sodass nur geringe Kontaktzeiten möglich sind.…”

Section: Ergebnisse Und Diskussionunclassified